
人 IFNA1/IFNA13 抗体对
01AB00145
The IFNA1 gene encodes the interferon alpha-1 protein, which is a member of the type I interferon family of cytokines. IFNA1 is primarily produced by cells of the immune system, such as B lymphocytes, plasmacytoid dendritic cells, and macrophages, in response to viral infections. The IFNA1 protein binds to the interferon alpha receptor (IFNAR), activating the JAK/STAT signaling pathway. This leads to the induction of interferon-stimulated genes that have antiviral effects and modulate the immune response. Dysregulation of IFNA1 and type I interferon signaling has been implicated in several autoimmune diseases, including systemic lupus erythematosus, rheumatoid arthritis, Sjögren's syndrome, and multiple sclerosis. Increased IFNA1 levels and interferon-stimulated gene expression are frequently observed in patients with these conditions and may contribute to inflammation and tissue damage.
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技术参数
- 靶点基因名
- IFNA1,IFNA13
- 蛋白别名
- interferon alpha 1,interferon alpha 13; IFNA1/IFNA13
- UniProt
- P01562
- 物种
- Human
产品详情
- 靶点名称
- IFNA1/IFNA13
- 蛋白名称
- interferon alpha 1,interferon alpha 13
- 蛋白别名
- Interferon alpha-1/13; IFN-alpha-1/13; Interferon alpha-D; LeIF D
- 靶点基因名
- IFNA1,IFNA13
- UniProt
- P01562
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
The IFNA1 gene encodes the interferon alpha-1 protein, which is a member of the type I interferon family of cytokines. IFNA1 is primarily produced by cells of the immune system, such as B lymphocytes, plasmacytoid dendritic cells, and macrophages, in response to viral infections. The IFNA1 protein binds to the interferon alpha receptor (IFNAR), activating the JAK/STAT signaling pathway. This leads to the induction of interferon-stimulated genes that have antiviral effects and modulate the immune response. Dysregulation of IFNA1 and type I interferon signaling has been implicated in several autoimmune diseases, including systemic lupus erythematosus, rheumatoid arthritis, Sjögren's syndrome, and multiple sclerosis. Increased IFNA1 levels and interferon-stimulated gene expression are frequently observed in patients with these conditions and may contribute to inflammation and tissue damage.